Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01185 (vasopressin)
 23,126 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Ischemia and reperfusion alter the reactivity of large coronary arteries, but the effect of ischemia and reperfusion on the coronary microcirculation has been less well defined. Elevated circulating levels of vasopressin are associated with cardiopulmonary bypass and numerous other clinical states in which vascular ischemia and reperfusion may occur. We examined the effects of ischemia with and without reperfusion on the responses to vasopressin of both large coronary arteries and coronary arterial microvessels. Studies were performed on vessels from control dogs (n = 8), dogs undergoing 1 hour of ischemia only (n = 8), and dogs undergoing 1 hour of ischemia followed with 1 hour of reperfusion (n = 9). Rings of proximal obtuse marginal coronary arteries distal to the site of circumflex coronary artery occlusion were studied in isolated organ chambers. Coronary microvessels (110 to 220 microns in diameter) were studied in a pressurized (20 mm Hg), no-flow state with a microvessel imaging apparatus and electronic dimension analyzer. Microvessels were preconstricted with the thromboxane A2 analog U46619. Responses of large vessel rings were studied in the nonpreconstricted state and after preconstriction with prostaglandin F2 alpha. Large vessel response to vasopressin was minimal and not altered by ischemia with or without reperfusion. In contrast, ischemia markedly affected the coronary microvascular response to vasopressin (10 to 1000 microU/ml). Control coronary microvessels constricted minimally to vasopressin (4% +/- 2% of the baseline diameter), while microvessels after either ischemia alone or ischemia followed by reperfusion constricted 22% +/- 5% and 21% +/- 3%, respectively (p less than 0.05 versus control for both). Hemoglobin, which inactivates the endothelium-derived relaxing factor, augmented microvascular constrictions to vasopressin in all groups to a similar extent. Relaxations to the endothelium-independent agent nitroglycerin were not altered by ischemia. Constrictions of the coronary microcirculation to vasopressin in conditions such as cardiopulmonary bypass or myocardial ischemia, in which circulating levels of vasopressin are increased, may predispose to persistent myocardial ischemia in the perioperative setting.
J Thorac Cardiovasc Surg 1992 Aug
PMID:Altered effects of vasopressin on the coronary circulation after ischemia. 149 97

Human atria through release of atrial natriuretic peptide play an important role in extracellular fluid homeostasis. This study investigates the perioperative role of atrial natriuretic peptide, renin, angiotensin, aldosterone, and vasopressin in patient response to cardiopulmonary bypass after coronary artery bypass operations. Serum levels of these hormones were measured, along with hemodynamic profiles, urine output, and urine electrolytes, before induction of anesthesia, after discontinuation of cardiopulmonary bypass, 1 hour postoperatively, and 3 hours postoperatively. Serum levels of atrial natriuretic peptide were found to be significantly elevated immediately after discontinuation of cardiopulmonary bypass. These elevations did not correspond temporally to elevated central venous pressure or tachycardia. Significant natriuresis and diuresis were observed during the first postoperative hour. This diuresis failed to correspond temporally with alterations noted in serum levels of atrial natriuretic peptide, renin, angiotensin, aldosterone, and vasopressin. The mechanism responsible for the increases in serum atrial natriuretic peptide and the postoperative natriuresis and diuresis after cardiopulmonary bypass remain unknown.
J Thorac Cardiovasc Surg 1992 Jun
PMID:Atrial natriuretic peptide may not play a role in diuresis and natriuresis after cardiac operations. 153 91

Systemically administered serotonin (5-HT) agonists have been suggested to act centrally to increase plasma renin activity (PRA) and arterial pressure (AP). To test this hypothesis, hemodynamic responses were determined in conscious male rats after intracerebroventricular (i.c.v.) or intravenous (i.v.) administration of the direct 5-HT agonist quipazine. When administered i.v., quipazine increased AP and PRA, and decreased renal blood flow (RBF); doses of quipazine i.c.v. that increased AP to a similar degree failed to increase PRA. The increase in PRA elicited by i.v. quipazine was not blocked by propranolol, suggesting non-neural mechanisms. The increase in AP and decrease in RBF elicited by i.v. quipazine were not eliminated by prazosin, enalapril, or a V1-vasopressin antagonist administered alone or in combination. LY 53857, a 5-HT2 antagonist that enters the central nervous system (CNS), blocked all responses to i.v. quipazine. In contrast, the peripheral 5-HT2 antagonist xylamidine blocked the renin and RBF responses, but only attenuated the pressor response to quipazine. These data suggest that quipazine can act in the CNS to increase AP, but when administered systemically quipazine also activates vascular 5-HT2 receptors to increase AP further and to decrease RBF. The increase in PRA caused by i.v. quipazine is secondary to renal hemodynamics and is unrelated to CNS actions of this drug.
J Cardiovasc Pharmacol 1990 Jan
PMID:Quipazine increases renin release by a peripheral hemodynamic mechanism. 168 63

The effects of pretreatment with atrial natriuretic factor (ANF) on the pressor responsiveness to injections of angiotensin II (ANGII), arginine vasopressin (AVP), and norepinephrine (NE), as well as the effect of pretreatment with ANGII on the hypotensive responses to ANF injection were studied in conscious sheep. The hemodynamic effects of ANF infusion (100 micrograms/h for 60 min) were also examined in animals pretreated with the angiotensin-converting enzyme (ACE) inhibitor, captopril. Infusion of ANF attenuated the pressor responsiveness to exogenous AII and NE, but caused no significant change in the blood pressure increases produced by vasopressin. In contrast, infusion of AII had no effect on the immediate hypotensive response to ANF injection. Infusion of ANF for 60 min produced similar hemodynamic actions in sheep during ACE inhibition as compared with the responses observed in normal sheep, although the reduction in cardiac output and increase in calculated total peripheral resistance was attenuated. Infusion of captopril increased plasma concentration of renin (PRC), and infusion of ANF produced no further change in PRC. In conclusion, the short-term cardiovascular responses to ANF infusion in conscious sheep are not mediated solely by inhibition of the renin-angiotensin system. However, ANF attenuates the pressor actions of pharmacologic doses of exogenous ANGII and NE. In contrast, the vasodepressor response to exogenous ANF injection was not altered in animals receiving ANGII infusion. This study suggests that ANF may be important in regulating the effects of endogenous vasoconstrictor hormones on blood pressure (BP).
J Cardiovasc Pharmacol 1990 Jan
PMID:Effects of atrial natriuretic factor on pressor responsiveness to angiotensin II, norepinephrine, and vasopressin in conscious sheep. 168 75

Adaptations to the effects of clonidine (CL) and rilmenidine (R) were studied during a 12-week training program (swimming) in spontaneously hypertensive rats (SHR) and Wistar-Kyoto (WKY) rats. Systolic blood pressure (SBP) was regularly measured during this period. Body weight (BW) was determined at the beginning and at the 12th week. Plasma parameters, cardiac determinations, vasopressin (pAVP), and plasma renin activity (PRA) were measured only at the end of the experiment. Both SBP and ponderal benefit were reduced by CL, R, and training. Contrary to beta-adrenoceptor blocking agents, we found no inhibition of the beneficial effect on SBP of training in combination with CL or R. Plasma and hypothalamic vasopressin were reduced by both drugs but only CL increased plasma renin activity (PRA) although its mechanisms of action are still not clearly understood. Our results suggest that CL and R as well as swim training can be considered as an effective countermeasure in SHR. Moreover, the heterogeneity of action of CL and R on some of the parameters tested is in favor of different pharmacological properties for these drugs.
J Cardiovasc Pharmacol 1990 Jan
PMID:Effects of swim training alone and in combination with clonidine and rilmenidine on blood pressure, plasma electrolytes, vasopressin, and renin activity in spontaneously hypertensive rats. 168 85

Experiments were performed on anesthetized (chloral hydrate) Wistar rats to determine the effect of vasopressin (VP) on cerebral blood flow (CBF), cerebral oxygen consumption (CMRO2), cerebrovascular resistance (CVR), and mean arterial blood pressure (MAP) before and after V1 or V2 VP receptor blockade. Influence of synthetic V2 receptor agonist (dVDAVP) on these variables was also tested. Intracarotid administration of 5 mU VP (Pitressin, n = 15) significantly increased CBF by 28% and CMRO2 by 27% and reduced CVR by 20% of control value. Intravenous (i.v.) infusion of dEt2AVP (V1 antagonist, 15 micrograms kg-1 h-1, n = 7) did not influence the effect of VP on CBF, CMRO2, and CVR but abolished MAP increase after VP. Intravenous (i.v.) infusion of d(CH2)5[D-Ile2,Abu4] AVP (V2 antagonist, 15 micrograms kg-1 h-1, n = 8) abolished the effect of VP on CBF, CMRO2, and CVR without changing its influence on MAP. Intracarotid administration of 12.5 ng dVDAVP (n = 7) increased CBF by 43% and CMRO2 by 29% and decreased CVR by 29% of control value. MAP was not affected. The results suggest that VP-induced CBF increase is, at least partly, caused by the rise of CMRO2 and mediated by V2-like receptors.
J Cardiovasc Pharmacol 1990 Apr
PMID:V2-like receptors mediate cerebral blood flow increase following vasopressin administration in rats. 169 87

It has been hypothesized that a decreased activity of vagal afferents might contribute to the activation of neurohumoral systems in congestive heart failure. Therefore, we studied the effects of vagal nerve blockade by local anesthesia on neurohormones in six conscious dogs before and after induction of heart failure by rapid right ventricular pacing (250 beats/min, 10 days). In healthy dogs, vagal blockade significantly increased plasma vasopressin levels (from 1.5 +/- .6 to 13.7 +/- 10.5 pg/ml, p less than 0.02), without significantly affecting plasma catecholamines and renin. After 10 days of pacing, mean arterial pressure and cardiac output were decreased, right atrial and pulmonary arterial pressures and plasma levels of norepinephrine, dopamine, and atrial natriuretic peptide were increased. In this state, vagal blockade significantly increased plasma renin activity (from 1.52 +/- .43 to 3.18 +/- .54 ngAI/ml/h, p less than 0.02) and plasma vasopressin (from 4.2 +/- 3.3 to 89.1 +/- 54.9 pg/ml, p less than 0.02), this increase being significantly higher than in healthy dogs. We conclude that in these dogs with low cardiac output state, which resembles early heart failure, vagal afferent activity is increased and effectively suppresses renin and vasopressin. This does not exclude the possibility that in later stages of heart failure vagal afferent dysfunction may develop, resulting in neurohumoral disinhibition.
J Cardiovasc Pharmacol 1990 Apr
PMID:Effects of vagal blockade on neurohumoral systems in conscious dogs with heart failure. 169 88

To gain insight with regard to the mode of action of calcium antagonists on the vasculature, we examined the effects of nifedipine, isradipine, felodipine, verapamil, gallopamil, and amlodipine on vasoconstrictor-induced prostacyclin synthesis in vitro. Cultured rat aortic smooth muscle cells were seeded after two to four passages in multiwell plates. After washing of the culture medium and a preincubation period, the cells were exposed for 1 h to either angiotensin II (Ang II) or arginine-vasopressin (AVP) at increasing concentrations between 10(-10)-10(-6) M with or without each calcium antagonist tested at 10(-6) M. At the end of the incubation period, the medium was aspirated, centrifuged, and assayed for its content of protein and of 6-keto-PGF1 alpha by radioimmunoassay. Ang II induced a 15-fold increase and AVP induced a fivefold increase of 6-keto-PGF1 alpha at 10(-6) M. None of the various calcium channel blockers tested showed a significant effect on this agonist-stimulated production of 6-keto-PGF1 alpha. Consequently, calcium-channel blockers with different chemical structure, although known to inhibit agonist-induced vasoconstriction, appear to preserve vasoconstrictor-induced production of prostacyclin, a potent vasodilator and an inhibitor of platelet aggregation.
J Cardiovasc Pharmacol 1990 Apr
PMID:Effect of different calcium channel blockers on angiotensin II- and vasopressin-induced prostacyclin biosynthesis in vascular smooth muscle cells. 169 90

After a single-blind, randomized, cross-over protocol using decaffeinated coffee in a control experiment, the effect of an oral 250-mg caffeine dose on plasma immunoreactive atrial natriuretic peptide (ANF) was assessed in eight healthy students who had been on a methylxanthine-free diet for 1 week. One to 2 h after caffeine ingestion, both systolic blood pressure (SBP) and diastolic BP (DBP) increased by 12 mm Hg while heart rate (HR) also tended to increase. An increase in diuresis and in urinary sodium, potassium, and osmol excretion was observed within 1 h. Decaffeinated coffee induced no change in any of these parameters. Plasma epinephrine (EPI) increased gradually from 16.6 +/- 3.2 pg/ml (mean +/- SEM) to 45.1 +/- 7.9 pg/ml within 2 h after caffeine ingestion, but did not change after decaffeinated coffee (p less than 0.001). Plasma norepinephrine (NE), renin activity (PRA), aldosterone, and vasopressin remained unchanged. Plasma ANF was measured by radioimmunoassay (RIA) using an extremely sensitive antiserum (Kd = 10(-12) M) after rapid and virtually complete (90-103%) extraction from plasma. In 0.2 ml plasma, the theoretical detection limit is 1.1 fmol/ml. Normal plasma ANF concentrations in supine subjects were 17.9 +/- 8.1 fmol/ml (mean +/- SD) and 11.0 +/- 3.3 fmol/ml in subjects in the upright position. Plasma ANF levels were not affected by coffee drinking. In conclusion, by using a new and sensitive assay for plasma ANF, we did not find that caffeine-induced diuresis is mediated by ANF.
J Cardiovasc Pharmacol 1990 May
PMID:Caffeine-induced diuresis and atrial natriuretic peptides. 169 26

The modification of endothelin effects by the calcium antagonist isradipine was investigated by infusion of 1.0 nM/kg endothelin, a dose known to cause profound vasoconstriction, into eight anesthetized rabbits, followed by an infusion of 10 micrograms/kg isradipine or its vehicle into four rabbits each. In a second series of experiments, only isradipine (same dose) or its vehicle was infused into six rabbits each. Endothelin increased blood pressure and caused systemic vasoconstriction, marked bradycardia, and cardiodepression (measured with a strain guage), yet decreased central venous pressure. The regional vascular effects (measured with microspheres) encompassed widespread vasoconstriction (especially to the kidneys, adrenals, stomach, cecum, and heart), but also a tendency for vasodilatation (hepatic artery). Isradipine decreased blood pressure in endothelin-treated and normal animals. It increased cardiac output more in the endothelin group. The interaction between endothelin and isradipine in the peripheral circulation was generally additive. Isradipine blunts many, but not all, endothelin effects, thus resembling the antivasoconstrictor effects of calcium antagonists against a variety of vasoconstrictor agents such as angiotensin II (Ang II) or vasopressin. Similar to these, endothelin appears to cause vasoconstriction by several mechanisms, one of which apparently involves L-channel activation. A specific interaction of endothelin with the L-channel appears unlikely.
J Cardiovasc Pharmacol 1990
PMID:Attenuation of endothelin-induced regional vasoconstriction by isradipine: a nonspecific antivasoconstrictor effect. 169 3


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